Elevated levels of 15-HpETE-PE after traumatic brain injury led to ferroptosis in the cerebral cortex and hippocampus, accompanied by increased expression of 15LO2 (a catalyst for the formation of protoferroporphyrin 15-oh-eicosapentaenoic acid) and depletion of GPX4, leading to cognitive impairment, effectively suggesting the possibility of ferroptosis (Wenzel et al., 2017). Here, GPX4 is linked to Cognitive impairment.